Much attention is now paid to investigation of the pathophysiologic processes occurring during the postreanimation period, and to discovering the causes of their development in order to make treatment more effective. Particular attention is focused on study of the state of the metabolic processes, as the degree to which they are impaired determines the seriousness and reversibility of the functional and morphologic alterations.
It is not a coincidence that, at the international symposia devoted to problems of management of the postreanimation period and prognostication and to the clinical pathophysiology of terminal states, several papers were devoted to the biochemical aspects of this important problem, greatest attention being correctly paid to oxidative processes, above all to changes in oxygen balance and in acid-base equilibrium.
Research carried out in our Laboratory has shown that, during the postreanimation period in patients with severe multiple injuries, and in cases of massive loss of blood, oxygen content can be low in the first five days in spite of stable arterial pressure, absence of clinically expressed respiratory insufficiency, and often even normal oxygen tension in arterial blood, and a high concentration of oxyhaemoglobin. A main reason for the development of oxygen lack in the organism in these states, it must be thought, is the fall in the concentration, and especially in the amount, of haemoglobin as a result of anaemia and the reduced volume of actively circulating erythrocytes.
The development of metabolic acidosis is most typical of terminal states. In the opinion of Laborit et al., it is not acidosis in general that has a negative effect on the course of the postreanimation period, but the acidosis due to a high blood level of lactic acid. The findings of a number of authors indicate that in cases of traumatic shock acidosis is a result of a discrepancy between the tissue’s increased demand for oxygen and the possibility of supplying it owing to the disturbance of circulation, in particular peripheral circulation, and to anaemia.
According to our findings, lasting uncompensated metabolic acidosis is observed in cases of III-IV degree traumatic shock and of massive loss of blood, only in combination with unstable arterial pressure and a sharp deficit in the volume of circulating blood. As the patient’s state deteriorates, acidosis progresses. When the acid-base equilibrium is determined in the mixed capillary blood obtained by pricking the soft tissue of the finger, blood pH fell to 7.19, standard bicarbonate content (SB) to 15.4, and base deficit (BE) to 11.8 mEq/litre in most patients who subsequently died in the first or second day. The sharp increase in total organic acid content to 24.1 mEq/litre against a standard 12 indicated a severe form of tissue hypoxia.
In patients who were successfully pulled out of the state of shock metabolic acidosis lasted for up to six or eight hours, in spite of stabilization of arterial pressure at a fairly high level, blood pH being 7.31, SB = 18.7, BE = —9.4. Disturbances of peripheral circulation, usually spasmic, were noted. At this time as a rule, it should be noted, massive haemotransfusion was continued and the necessary surgical intervention made. After ten or twelve hours of treatment, when the loss of blood had, in the main, been compensated, the indices of acid-base equilibrium had become normal, although the total organic acid concentration remained high.
Later, at the end of the first day and beginning of the second, an accumulation of bases was noted, and metabolic acidosis gave way to metabolic alkalosis. Since the rise in CO2 tension was slower in several patients than the accumulation of bases and a reserve of bicarbonates, the alkalosis was decompensated. The graver the patient’s condition the more often were subcompensation and decompensation observed.
In cured patients, as a rule, there was gradual compensation of metabolic alkalosis. The maximum accumulation of bases occurred during the third day. Under the influence of the therapy applied, these disturbances were gradually eliminated, but acid-base equilibrium was only normalized in the course of 20 days, occasionally longer.
In patients who died during the third or fourth day, or a little later, in spite of the treatment administered, metabolic alkalosis progressed and became decompensated: blood pH rose to 7.48; SB to 31.2, and BE to +7.94 mEq/litre. Total organic acid content increased simultaneously, reaching 36-38 mEq/litre in some patients.
In illustration of this we have included data on the changes in acid-base equilibrium for several patients who were under observation in the reanimation department of the Hospital.
The disturbances of acid-base equilibrium described developed on a background of marked anaemia, hypoproteinaemia, and hypovolemia.
These data confirm that metabolic acidosis is typical of patients in states of severe shock or in the terminal state. Once they have been brought out of it, metabolic acidosis gradually gives way to metabolic alkalosis, with a simultaneous increase in the total plasma concentration of organic acids. The more serious the patient’s state the higher is the degree of metabolic alkalosis.
Although the development of metabolic acidosis during the postreanimation period has already been widely discussed in the literature, there are only isolated works, it should be noted, on metabolic alkalosis. Some authors consider the main cause of metabolic alkalosis to be lack of potassium in the organism. Salenius explained its development with loss of blood by the entry of more basic liquid from the extracellular spaces into the blood stream.
But there are still no clear findings in the literature explaining the pathogenesis of this complication in the presence of high plasma concentration of organic acids.
In order to get a more detailed explanation of the causes of metabolic alkalosis in patients with severe traumatic damage, we correlated certain haemodynamic indices with the state of acid-base equilibrium, and found that given a satisfactory or increased volume of circulating blood, especially of plasma, the indices of acid-base equilibrium did not differ essentially from normal. When the volume of circulating blood was reduced on average by 10.8 per cent and by 35.1 per cent the overwhelming majority of patients developed metabolic alkalosis.
The fact that there was a more marked reduction in the volume of circulating plasma, and oliguria, in all patients with metabolic alkalosis, deserves attention. But the haematocrit index remained normal in several cases. The average haematocrit index was of 25.9 units, and the volume of circulating blood 39.5 ml/kg, and of plasma 29.4 ml/kg. When the haematocrit index was 37.2 units, the volume of circulating blood was 44.2 ml/kg, and of plasma 27.4 ml/kg. These findings allow us to suppose that the accumulation of bases in the blood is a result of hypovolemia, especially of a reduction in the volume of circulating plasma. At the same time a high plasma concentration of sodium bicarbonate is not always indicative of a large reserve of bases in the vessels, since, with a significant decrease in the volume of plasma, the amount of bases may also be reduced despite their high concentration.
As regards electrolyte balance, the reports in the literature were highly contradictory until recently.
Many authors consider that hyperkalemia is typical of severe traumatic lesions; whereas, in the opinion of others, it is hypokalemia that develops.
Research into the state of the electrolyte balance in patients with traumatic lesions using flame photometry showed that plasma potassium concentration varied widely, from 4.5 to 2.0 mEq/litre. But its amount in the circulating blood was reduced by approximately one third below normal, independently of concentration. The quantity of potassium eliminated in the urine in the first 24 hours remained within normal limits or increased slightly, and decreased during the next two days. The reduced excretion of potassium in the urine was in all likelihood due to cells being impoverished of it by the considerably increased excretion in the first 24 hours, with a low plasma level and very limited external supply.
The fall in erythrocyte potassium content from a normal 76-100 mEq/litre to 51 to 66 mEq/litre is an indirect indication that its content in the tissues has decreased. Plasma and urine sodium concentration though also reduced, was much less so than the potassium concentration. But excretion of sodium with the urine fell considerably. The development of hyponatriuria is apparently the result of its retention in the organism and accumulation in the tissues. The accumulation of sodium in the organism can be promoted (a) by an increase in its reabsorption in the kidney tubules as a result of a reflex increase in aldosterone secretion in response to reduction of the volume of circulating blood, and (b) by its introduction from outside in transfusates.
Correlation of the changes in electrolyte balance with the course of the illness allows us to conclude that prolonged hypokaliaemia and hypokaliuria in spite of the administration of potassium preparations are typical of an unfavourable outcome of treatment. Progressive kaliuria and retention of sodium in the organism are also poor prognostic signs.
Thus the laboratory research into several metabolic processes taking place in the organism in the postreanimation period gives grounds for supposing that the development of metabolic alkalosis is linked to a considerable extent with hypovolaemia and severe disturbances of cell electrolyte balance, that is to say with accumulation of sodium ions and impoverishment of potassium ions.
When alkalosis is prolonged there are, as we know, difficulties in oxyhaemoglobin dissociation and continuation of a spastic state in the peripheral vessels that, in turn, aggravates tissue hypoxia. And as already indicated above, with stable progressive decompensated alkalosis the prognosis, as a rule, is unfavourable in spite of the most vigorous complex treatment. The causes of the development of metabolic alkalosis and the means of preventing and treating it, all await further study.
It is quite obvious, however, that the most practical form of prophylaxis is vigorous therapy in the early stages of treatment: rapid making up of the volume of circulating blood, elimination of hypoproteinaemia and metabolic acidosis, normalization of peripheral circulation and of respiration, systematic application of sufficient quantities of potassium chloride and limiting of sodium. When the beginning of treatment is delayed, the organism’s compensatory reactions directed at restoring its fluid volume and reserves of the main plasma cation, valuable as they are initially, lead to the development of a pathological stage of metabolic alkalosis.